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Omics for Metabolic Mysfunctions
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Omics for Metabolic Mysfunctions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 17619

Special Issue Editor

Dr. Abdelnaby Khalyfa

E-Mail Website
Guest Editor
Department of Child Health, School of Medicine, University of Missouri, Columbia, MO 65211, USA
Interests: genetic markers; sleep apnea; exosomes; single cell; snRNA-seq; metabolic dysfunction; animal models for sleep apnea
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiometabolic disease is among the leading causes of morbidity and mortality worldwide and is a significant burden on the healthcare system. The use of high-throughput omics technologies has led to the rapid discovery of many candidate biomarkers. Systems biology integrated high-throughput multi-omics approach has been dedicated to understanding complete molecular biosignature of health and disease. Omics-based integrative identification and characterization of biomarker targets and their clinical translations are essential to developing comprehensive profiling, risk stratification, future cell-targeted early interventional and therapeutic strategies. This Special Issue will include the omics approaches such as genomics, transcriptomics, proteomics, lipidomics, or metabolomics to study the biological pathways and interaction at the cells and exosomes levels. Both human and animal model multi-omics will provide researchers with a greater understanding of the flow of information, from the original cause of the disease (genetic, environmental, or developmental) to the functional consequences or relevant interactions. We are aiming to develop omics-based discriminatory biomarkers for early detection, as well as novel targeted interventional and therapeutic strategies that are crucial for a personalized healthy life as well as disease management including cardiometabolic disease. Compared to single omics interrogations, multi-omics can provide a better understanding of the biological information, from the original cause of the disease (genetic, environmental, or developmental). In this Special Issue, we are aiming to broadly address topics from understanding the basic science and clinical applications in cardiovascular regeneration and disease treatment as well as in vitro disease modeling approaches.

Dr. Abdelnaby Khalyfa
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • omics
  • genomics
  • transcriptomics
  • proteomics
  • metabolomics
  • microbiome
  • extracellular vesicles
  • exosomes
  • sleep
  • cardiovascular diseases

Published Papers (6 papers)

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Research

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18 pages, 44112 KiB  
Article
Derangements and Reversibility of Energy Metabolism in Failing Hearts Resulting from Volume Overload: Transcriptomics and Metabolomics Analyses
by Ying-Chang Tung, Mei-Ling Cheng, Lung-Sheng Wu, Hsiang-Yu Tang, Cheng-Yu Huang, Gwo-Jyh Chang and Chi-Jen Chang
Int. J. Mol. Sci. 2022, 23(12), 6809; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126809 - 18 Jun 2022
Cited by 2 | Viewed by 1643
Abstract
Derangements in cardiac energy metabolism have been shown to contribute to the development of heart failure (HF). This study combined transcriptomics and metabolomics analyses to characterize the changes and reversibility of cardiac energetics in a rat model of cardiac volume overload (VO) with [...] Read more.
Derangements in cardiac energy metabolism have been shown to contribute to the development of heart failure (HF). This study combined transcriptomics and metabolomics analyses to characterize the changes and reversibility of cardiac energetics in a rat model of cardiac volume overload (VO) with the creation and subsequent closure of aortocaval fistula. Male Sprague–Dawley rats subjected to an aortocaval fistula surgery for 8 and 16 weeks exhibited characteristics of compensated hypertrophy (CH) and HF, respectively, in echocardiographic and hemodynamic studies. Glycolysis was downregulated and directed to the hexosamine biosynthetic pathway (HBP) and O-linked-N-acetylglucosaminylation in the CH phase and was further suppressed during progression to HF. Derangements in fatty acid oxidation were not prominent until the development of HF, as indicated by the accumulation of acylcarnitines. The gene expression and intermediates of the tricarboxylic acid cycle were not significantly altered in this model. Correction of VO largely reversed the differential expression of genes involved in glycolysis, HBP, and fatty acid oxidation in CH but not in HF. Delayed correction of VO in HF resulted in incomplete recovery of defective glycolysis and fatty acid oxidation. These findings may provide insight into the development of innovative strategies to prevent or reverse metabolic derangements in VO-induced HF. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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21 pages, 5520 KiB  
Article
Tamoxifen Exerts Anticancer Effects on Pituitary Adenoma Progression via Inducing Cell Apoptosis and Inhibiting Cell Migration
by Tingting Lv, Zirui Zhang, Haoying Yu, Shuyue Ren, Jingrong Wang, Shang Li and Lan Sun
Int. J. Mol. Sci. 2022, 23(5), 2664; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052664 - 28 Feb 2022
Cited by 10 | Viewed by 2075
Abstract
Although pituitary adenomas are histologically benign, they are often accompanied by multiple complications, such as cardiovascular disease and metabolic dysfunction. In the present study, we repositioned the Food and Drug Administration -approved immune regulator tamoxifen to target STAT6 based on the genomics analysis [...] Read more.
Although pituitary adenomas are histologically benign, they are often accompanied by multiple complications, such as cardiovascular disease and metabolic dysfunction. In the present study, we repositioned the Food and Drug Administration -approved immune regulator tamoxifen to target STAT6 based on the genomics analysis of PAs. Tamoxifen inhibited the proliferation of GH3 and AtT-20 cells with respective IC50 values of 9.15 and 7.52 μM and increased their apoptotic rates in a dose-dependent manner. At the molecular level, tamoxifen downregulated phosphorylated PI3K, phosphorylated AKT and the anti-apoptotic protein Bcl-2 and increased the expression of pro-apoptotic proteins p53 and Bax in GH3 and AtT-20 cells. Furthermore, tamoxifen also inhibited the migration of both cell lines by reprogramming tumor-associated macrophages to the M1 phenotype through STAT6 inactivation and inhibition of the macrophage-specific immune checkpoint SHP1/SHP. Finally, administration of tamoxifen (20, 50, 100 mg·kg−1·d−1, for 21 days) inhibited the growth of pituitary adenomas xenografts in nude mice in a dose-dependent manner. Taken together, tamoxifen is likely to be a promising combination therapy for pituitary adenomas and should be investigated further. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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Graphical abstract

24 pages, 27654 KiB  
Article
Monocarboxylate Transporter-2 Expression Restricts Tumor Growth in a Murine Model of Lung Cancer: A Multi-Omic Analysis
by Abdelnaby Khalyfa, Zhuanhong Qiao, Murugesan Raju, Chi-Ren Shyu, Lyndon Coghill, Aaron Ericsson and David Gozal
Int. J. Mol. Sci. 2021, 22(19), 10616; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910616 - 30 Sep 2021
Cited by 4 | Viewed by 3277
Abstract
Monocarboxylate transporter 2 (MCT2) is a major high-affinity pyruvate transporter encoded by the SLC16A7 gene, and is associated with glucose metabolism and cancer. Changes in the gut microbiota and host immune system are associated with many diseases, including cancer. Using conditionally expressed MCT2 [...] Read more.
Monocarboxylate transporter 2 (MCT2) is a major high-affinity pyruvate transporter encoded by the SLC16A7 gene, and is associated with glucose metabolism and cancer. Changes in the gut microbiota and host immune system are associated with many diseases, including cancer. Using conditionally expressed MCT2 in mice and the TC1 lung carcinoma model, we examined the effects of MCT2 on lung cancer tumor growth and local invasion, while also evaluating potential effects on fecal microbiome, plasma metabolome, and bulk RNA-sequencing of tumor macrophages. Conditional MCT2 mice were generated in our laboratory using MCT2loxP mouse intercrossed with mCre-Tg mouse to generate MCT2loxP/loxP; Cre+ mouse (MCT2 KO). Male MCT2 KO mice (8 weeks old) were treated with tamoxifen (0.18 mg/g BW) KO or vehicle (CO), and then injected with mouse lung carcinoma TC1 cells (10 × 105/mouse) in the left flank. Body weight, tumor size and weight, and local tumor invasion were assessed. Fecal DNA samples were extracted using PowerFecal kits and bacterial 16S rRNA amplicons were also performed. Fecal and plasma samples were used for GC−MS Polar, as well as non-targeted UHPLC-MS/MS, and tumor-associated macrophages (TAMs) were subjected to bulk RNAseq. Tamoxifen-treated MCT2 KO mice showed significantly higher tumor weight and size, as well as evidence of local invasion beyond the capsule compared with the controls. PCoA and hierarchical clustering analyses of the fecal and plasma metabolomics, as well as microbiota, revealed a distinct separation between the two groups. KO TAMs showed distinct metabolic pathways including the Acetyl-coA metabolic process, activation of immune response, b-cell activation and differentiation, cAMP-mediated signaling, glucose and glutamate processes, and T-cell differentiation and response to oxidative stress. Multi-Omic approaches reveal a substantial role for MCT2 in the host response to TC1 lung carcinoma that may involve alterations in the gut and systemic metabolome, along with TAM-related metabolic pathway. These findings provide initial opportunities for potential delineation of oncometabolic immunomodulatory therapeutic approaches. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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Review

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21 pages, 883 KiB  
Review
Precision Nephrology in Patients with Diabetes and Chronic Kidney Disease
by Michele Provenzano, Federica Maritati, Chiara Abenavoli, Claudia Bini, Valeria Corradetti, Gaetano La Manna and Giorgia Comai
Int. J. Mol. Sci. 2022, 23(10), 5719; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105719 - 20 May 2022
Cited by 5 | Viewed by 3065
Abstract
Diabetes is the leading cause of kidney failure and specifically, diabetic kidney disease (DKD) occurs in up to 30% of all diabetic patients. Kidney disease attributed to diabetes is a major contributor to the global burden of the disease in terms of clinical [...] Read more.
Diabetes is the leading cause of kidney failure and specifically, diabetic kidney disease (DKD) occurs in up to 30% of all diabetic patients. Kidney disease attributed to diabetes is a major contributor to the global burden of the disease in terms of clinical and socio-economic impact, not only because of the risk of progression to End-Stage Kidney Disease (ESKD), but also because of the associated increase in cardiovascular (CV) risk. Despite the introduction of novel treatments that allow us to reduce the risk of future outcomes, a striking residual cardiorenal risk has been reported. This risk is explained by both the heterogeneity of DKD and the individual variability in response to nephroprotective treatments. Strategies that have been proposed to improve DKD patient care are to develop novel biomarkers that classify with greater accuracy patients with respect to their future risk (prognostic) and biomarkers that are able to predict the response to nephroprotective treatment (predictive). In this review, we summarize the principal prognostic biomarkers of type 1 and type 2 diabetes and the novel markers that help clinicians to individualize treatments and the basis of the characteristics that predict an optimal response. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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23 pages, 629 KiB  
Review
OMICS in Chronic Kidney Disease: Focus on Prognosis and Prediction
by Michele Provenzano, Raffaele Serra, Carlo Garofalo, Ashour Michael, Giuseppina Crugliano, Yuri Battaglia, Nicola Ielapi, Umberto Marcello Bracale, Teresa Faga, Giulia Capitoli, Stefania Galimberti and Michele Andreucci
Int. J. Mol. Sci. 2022, 23(1), 336; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010336 - 29 Dec 2021
Cited by 7 | Viewed by 2930
Abstract
Chronic kidney disease (CKD) patients are characterized by a high residual risk for cardiovascular (CV) events and CKD progression. This has prompted the implementation of new prognostic and predictive biomarkers with the aim of mitigating this risk. The ‘omics’ techniques, namely genomics, proteomics, [...] Read more.
Chronic kidney disease (CKD) patients are characterized by a high residual risk for cardiovascular (CV) events and CKD progression. This has prompted the implementation of new prognostic and predictive biomarkers with the aim of mitigating this risk. The ‘omics’ techniques, namely genomics, proteomics, metabolomics, and transcriptomics, are excellent candidates to provide a better understanding of pathophysiologic mechanisms of disease in CKD, to improve risk stratification of patients with respect to future cardiovascular events, and to identify CKD patients who are likely to respond to a treatment. Following such a strategy, a reliable risk of future events for a particular patient may be calculated and consequently the patient would also benefit from the best available treatment based on their risk profile. Moreover, a further step forward can be represented by the aggregation of multiple omics information by combining different techniques and/or different biological samples. This has already been shown to yield additional information by revealing with more accuracy the exact individual pathway of disease. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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19 pages, 1346 KiB  
Review
Applying Proteomics and Integrative “Omics” Strategies to Decipher the Chronic Kidney Disease-Related Atherosclerosis
by Joanna Tracz and Magdalena Luczak
Int. J. Mol. Sci. 2021, 22(14), 7492; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147492 - 13 Jul 2021
Cited by 6 | Viewed by 3532
Abstract
Patients with chronic kidney disease (CKD) are at increased risk of atherosclerosis and premature mortality, mainly due to cardiovascular events. However, well-known risk factors, which promote “classical” atherosclerosis are alone insufficient to explain the high prevalence of atherosclerosis-related to CKD (CKD-A). The complexity [...] Read more.
Patients with chronic kidney disease (CKD) are at increased risk of atherosclerosis and premature mortality, mainly due to cardiovascular events. However, well-known risk factors, which promote “classical” atherosclerosis are alone insufficient to explain the high prevalence of atherosclerosis-related to CKD (CKD-A). The complexity of the molecular mechanisms underlying the acceleration of CKD-A is still to be defied. To obtain a holistic picture of these changes, comprehensive proteomic approaches have been developed including global protein profiling followed by functional bioinformatics analyses of dysregulated pathways. Furthermore, proteomics surveys in combination with other “omics” techniques, i.e., transcriptomics and metabolomics as well as physiological assays provide a solid ground for interpretation of observed phenomena in the context of disease pathology. This review discusses the comprehensive application of various “omics” approaches, with emphasis on proteomics, to tackle the molecular mechanisms underlying CKD-A progression. We summarize here the recent findings derived from global proteomic approaches and underline the potential of utilizing integrative systems biology, to gain a deeper insight into the pathogenesis of CKD-A and other disorders. Full article
(This article belongs to the Special Issue Omics for Metabolic Mysfunctions)
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